(N/A) neural signal reaching the neuromuscular junction releases a neurotransmitter (Acetylcholine) which generates an action potential in the sarcolemma. This spreads through the muscle fibre and causes the release of $Ca^{++}$ (calcium ions) into the sarcoplasm.
Increase in $Ca^{++}$ level leads to the binding of $Ca^{++}$ with a subunit of troponin on actin filaments,thereby removing the masking of active sites for myosin.
Utilising the energy from $ATP$ hydrolysis,the myosin head now binds to exposed active sites on actin to form a cross-bridge.
This pulls the attached actin filaments towards the centre of the '$A$' band. The '$Z$' line attached to these actins are also pulled inwards,thereby causing a shortening of the sarcomere,i.e.,contraction.
It is clear from the above steps that during the shortening of the muscle (contraction),the '$I$' bands get reduced,whereas the '$A$' band retains its length.
The myosin,releasing the $ADP$ and $P_i$,goes back to its relaxed state. $A$ new $ATP$ binds and the cross-bridge is broken.
The $ATP$ is again hydrolysed by the myosin head and the cycle of cross-bridge formation and breakage is repeated,causing further sliding. The process continues until the $Ca^{++}$ ions are pumped back to the sarcoplasmic cisternae,resulting in the masking of actin filaments. This causes the return of '$Z$' lines back to their original position (i.e.,relaxation).